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Neuroanatomical theories of ADHD investigate possible causation within
th~ortical
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structures of the brain. Many of these theories are based on comparisons between
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certain clinical populations, in particular those patients with lesions to particular regions of the brain, and children with ADHD. Evidence for these theories are obtained by recording structural anomalies in the brain using sophisticated technology such as those listed earlier,as well as a battery of neuropsychologicaltests.
3.4.2.1. Frontal Lobe and Parietal Lobe Theories
The origins of frontal lobe theory can be traced to the 1930s when practitioners and researchers observed behavioural similarities between patients with frontal lobe
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lesions and children with ADHD symptoms (Levin, 1938, as cited in Aman,Roberts,
& Pennington, 1998). The frontal lobes,in particular the prefrontal regions,not only
~id working memory, but are also instrumental in executive functioning. These include developing and implementing cognitive goal-directed strategies for problem solving that are flexible in response to environmental cues, by controlling impulses and inhibiting prepotent responses. For example, Milner (1964, as cited in Kolb &
Whishaw, 1996) demonstrated how patients with frontal lobe lesions failed to change response strategies in the Wisconsin Card Sorting Test,despite articulating that they were aware that the requisite for success on the tasks had changed as the task progressed. Another study by Milner also suggested that the impairment in response inhibition tends to increase risk-taking behaviour. Patients ignored the buzzer that signaled when errors were made in tests of stylus-maze learning.Instead of changing their responses upon hearingthe buzzer, patients not only continued the test but also made more errors (as cited in Kolb & Whishaw, 1996). This example also demonstrates rigidity in decision-making processes. Frontal lobe patients displayed similar loss of response inhibition when they were unable to inhibit reading the words as opposed to identifying the colour in which the words were written in,in the Stroop Test (Perret, 1974,as cited in Kolb & Whishaw).
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The right parietal/10be theory is a more recent theory that is also based on
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. .-observations of similar attentional deficits in children diagnosed with ADHD and patients with right parietal lobe damage. The parietal lobes integrate sensory input from the somatic and visual regions of the brain as well as from other sensory regions. The posterior parietal cortex plays an important role in accurate visuallyguided motor
activity,spatial perception and spatial attention (Anderson, 1988,as cited in Aman. et aI., 1998). Choosing which utensil to use from an array of cutlery when eating at a restaurant is a simple example of this function.The right parietal lobe appears to be most reliably associated with deficits inthese functions, based on the frequencyand severity of deficits associated with lesions to the right hemisphere. In addition, problems inthis region may lead to visual neglect.
Neurobiological evidence exists to support both frontal lobe and parietal lobe theories.
Frontal lobes are functionally asymmetrical (Kolb & Whishaw, 1996). Using high resolution MRI,Hynd, et ai,(1990,as cited in Aman,et. ai, 1998)found that children with ADHD appear to have symmetrical anterior regions, unlike normal control children who appear to have asymmetrical frontal lobes, with the left anterior region being smaller than the right. In addition,Hynd,et al.(1993,as cited inAman,et al.) found reversed patterns of asymmetry on the head of the
caudate ~leus,
a portion of" '- - - - . i - > -
the basal ganglia that is heavily connected to the prefrontal cortex:the left region was smaller than the right in children diagnosed as having ADHD, in comparison to normal controls.Hynd,
.-
et al. (1991) have also found that areas of the corpus callosum containing fibres connecting anterior (frontal) and posterior (parietal) cortical regions in the left hemispheres are smaller in ADHD than in normal controls.3.4.3.Genetic Theories
Parker (1992,as citedinLerner, et aI., 1995) argues that heredity is the most common cause of ADHD. In fact there is strong evidence to suggest that there is a genetic predisposition to ADHD.Three types of studies have been used to determine the role
and extent of genetic factors in the aetiology of ADHO.These are family studies. twin studies, and adoption studies. Wender (1995) provides a very detailed and comprehensive account of major studies done in these three categories. Although Diller (1998) does not negate the existence of a genetic link to ADHD, he cautions against placing too much emphasis on it at the cost of ignoring other contributing aetiologies.
3.4.3.1. Family History Studies
A family history forms part of the initial assessment in the diagnosis of ADHO. It is often found that close family members show similar patterns of attentional problems (Seidman, et aI., 1997). In an earlier study by Seidman,et al. (1995) it was found that boys who were diagnosed as having ADHD and with a family history of ADHD performed more poorly on some neuropsychological tasks, than boys who were diagnosed as having ADHD but with no family history of ADHO.This implies that a genetic link may be associated with the disorder. Family studies attempt to find evidence to support this hypothesis.Furthermore they seek to determine if there is an increased frequency in the amount and type of psychopathology in the biological relatives of children with ADHD. Barkley (1990) proposed that up to 32% of parents of children with ADHO also exhibit symptoms of the disorder.
Neurochemical evidence exists to support the genetic theory. Zametkin, et aI.,found that adults who were diagnosed as having ADHD and.who were parents of children who were also diagnosed as having ADHD, displayed abnormalities of cerebral
metabolism in the prefrontal and premotor areas of the frontal lobe (as cited in Seidman, et al.. 1997).
Of the many criticisms levied against earlier studies, perhaps the most pertinent relates to the issue of comorbidity. Early studies failed to draw samples from homogenous groups, neither were these groups randomly selected. The existence of comorbid disorders in the research groups was highly probable. As discussed in· Chapter Two, comorbid disorders share many similar behavioural characteristics as ADHD. It is possible that retrospective assessments and diagnosis of ADHD among adults may have been based on the presence of other disorders (Wender, 1995).
3.4.3.2.Twin Studies
Twin studies essentially tackle the age-old nature versus nurture debate. These studies are based on the hypothesis that there is likely to be a higher prevalence of the disorder among monozygotic (identical) twins than dizygotic (fraternal) twins because monozygotic twins have identical genetic material. Studies comparing identical and fraternal twins strongly suggest that an 'ADHD personality' is inherited. In a longitudinal study of twins reared apart, Goodman & Stevenson (1989) found that identical twins displayed similar levels of hyperactivity despite being reared apart.
Fraternal twins were similar to normal children in the likelihood of displaying hyperactivity.
3.4.3.3.Adoption Studies
Although fraught with methodological problems similar to those contained in other types of genetic studies, adoption studies provide more solid and convincing evidence for a genetic basis for ADHD, thereby suggesting a limited influence of environmental factors. Adoption studies have made significant contributions to the understanding of the aetiologies of the disorder. The finding that the incidence of ADHD in adopted children is higher than for biological children strengthens the genetic theory of ADHD. Thisimplies that the biological parents of the adopted children were likely to have displayed ADHD symptoms as well (Silver, 1992, as cited in Lerner, et al, 1995). Furthermore, these studies suggest that ADHD occurs in clusters within families, affecting certain groups of members, such as fathers and sons (Diller, 1998). This may account for the higher prevalencerate among males.